Background/Case Studies: We present a case of a 64-y-old O pos Marshallese-speaking Pacific Islander female of Polynesian descent (Marshall Islands) who presented to the ED with lobar pneumonia. Lab studies showed hgb/hct 6.9 g/dL/20.7%. Initial Type & Screen (T&S) on 4/2022 O pos, negative antibody screen. Transfused 1 O pos PRBC. After transfusion subsequent testing showed patient developed an anti-Scianna 3 (anti-Sc3) red cell antibody. Transfused 5 PRBCs from 4/2022 – 8/2022.
Study
Design/Methods: ABO typing, direct antiglobulin test (DAT)tube method, indirect antiglobulin test and antibody identification [polyethylene glycol (PEG) and Gel automation testing]. Samples were sent out to immunohematology reference labs (IRL) for antibody identification with adsorption and neutralization techniques. DNA was isolated from peripheral blood (QIAGEN). Genotyping included: HEA Beadchip (Werfen); and amplification and sequencing of SC exons 4 and 12.
Results/Findings: : Initial ED laboratory testing revealed that the patient was group O, Rh-positive, and antibody screen negative with no signs of active bleeding. Low hgb/hct thought due to CKD. Patient transfused 1 PRBC with next day hgb 8.5. T&S 6 days later showed a positive antibody screen, Ab identification result was Antibody of Undetermined Specificity (AUS), DAT pos for IgG and C3d, elution neg. Transfused 1 AHG Gelcrossmatch compatible RBC. 109 days later the patient had another T&S performed. Panagglutination was detected in plasma and elution, DAT pos for IgG only. IRL titer reactivity was 64. Panagglutination was removed with allo adsorptions but not auto absorptions. Patient transfused 1 AHG Gel incompatible PRBC based on clinical need. On days 112 & 116 patient transfused 2 more AHG Gel INCOMP PRBCs. No signs of hemolysis using, T bili, LDH, AST, ALT indicators although Hgb never stayed increased for more than 1 day. Day 122 sample sent to another IRL that used neutralization and SC:-1,-2,-3 cells for identification. Patient HEA genotype showed patient to be Sc1+ but DNA sequencing determined the patient to be SC*01N.02/01N.02 which is predicted to be SC null phenotype SC:-1,-2,-3. No further transfusions were given to this patient at our facility due to inability to locate Sc3 negative PRBCs and patient apparent stabilization of hgb in mid 5s to low 6s. Conclusions: Anti Sc3 are known to cause “No to mild/delayed transfusion reaction” per “The Blood Group Antigen FactsBook” 3rd edition by Reed. Routine hemolysis chemistries were within the normal limits except for one elevated LDH 101 days post 2nd PRBC. Hgb boost did not last longer than 1 or 2 days. Since Sc3 neg units were unable to be located, future guidance was not to transfuse unless critical. Patient seemed to stabilize at hgb of approximately 6 g/dL.
